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A magas tesztoszteronkoncentráció nem fokozza a prosztatarák kialakulásának veszélyét. Valószínűleg éppen ellenkezőleg, az alacsony hormonszíntű férfiak kockázata nagyobb és a kialakuló tumor is veszélyesebb.<ref name="pmid19011298">{{cite book | vauthors = Morgentaler A, Schulman C | chapter = Testosterone and prostate safety | volume = 37 | pages = 197–203 | year = 2009 | pmid = 19011298 | doi = 10.1159/000176054 | isbn = 978-3-8055-8622-1 | series = Frontiers of Hormone Research | title = Advances in the Management of Testosterone Deficiency }}</ref><ref>{{cite journal | vauthors = Rhoden EL, Averbeck MA, Teloken PE | title = Androgen replacement in men undergoing treatment for prostate cancer | journal = The Journal of Sexual Medicine | volume = 5 | issue = 9 | pages = 2202–08 | date = Sep 2008 | pmid = 18638000 | doi = 10.1111/j.1743-6109.2008.00925.x }}</ref><ref>{{cite journal | vauthors = Morgentaler A, Traish AM | title = Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth | journal = European Urology | volume = 55 | issue = 2 | pages = 310–20 | date = Feb 2009 | pmid = 18838208 | doi = 10.1016/j.eururo.2008.09.024 }}</ref> Idős férfiakban a tesztoszteron közvetetten segít fenntartani a szív- és érrendszer egészségét azzal, hogy gátolja az izptömeg elvesztését, gátolja az elhízást és csökkenti a koleszterinszintet.<ref name="pmid18488876">{{cite journal | vauthors = Stanworth RD, Jones TH | title = Testosterone for the aging male; current evidence and recommended practice | journal = Clinical Interventions in Aging | volume = 3 | issue = 1 | pages = 25–44 | year = 2008 | pmid = 18488876 | pmc = 2544367 | doi = 10.2147/CIA.S190}}</ref> Nők esetében a magas androgénszint együtt járhat a szabálytalan menstruációs ciklussal.<ref name="pmid17039468">{{cite journal | vauthors = Van Anders SM, Watson NV | title = Menstrual cycle irregularities are associated with testosterone levels in healthy premenopausal women | journal = American Journal of Human Biology | volume = 18 | issue = 6 | pages = 841–44 | year = 2006 | pmid = 17039468 | doi = 10.1002/ajhb.20555 | url = https://deepblue.lib.umich.edu/bitstream/2027.42/83925/1/menstrual_cycle_irregularities_are_associated_with_testosterone_levels_in_healthy_premenopausal_women.pdf | hdl = 2027.42/83925 }}</ref>
A magas tesztoszteronkoncentráció nem fokozza a prosztatarák kialakulásának veszélyét. Valószínűleg éppen ellenkezőleg, az alacsony hormonszíntű férfiak kockázata nagyobb és a kialakuló tumor is veszélyesebb.<ref name="pmid19011298">{{cite book | vauthors = Morgentaler A, Schulman C | chapter = Testosterone and prostate safety | volume = 37 | pages = 197–203 | year = 2009 | pmid = 19011298 | doi = 10.1159/000176054 | isbn = 978-3-8055-8622-1 | series = Frontiers of Hormone Research | title = Advances in the Management of Testosterone Deficiency }}</ref><ref>{{cite journal | vauthors = Rhoden EL, Averbeck MA, Teloken PE | title = Androgen replacement in men undergoing treatment for prostate cancer | journal = The Journal of Sexual Medicine | volume = 5 | issue = 9 | pages = 2202–08 | date = Sep 2008 | pmid = 18638000 | doi = 10.1111/j.1743-6109.2008.00925.x }}</ref><ref>{{cite journal | vauthors = Morgentaler A, Traish AM | title = Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth | journal = European Urology | volume = 55 | issue = 2 | pages = 310–20 | date = Feb 2009 | pmid = 18838208 | doi = 10.1016/j.eururo.2008.09.024 }}</ref> Idős férfiakban a tesztoszteron közvetetten segít fenntartani a szív- és érrendszer egészségét azzal, hogy gátolja az izptömeg elvesztését, gátolja az elhízást és csökkenti a koleszterinszintet.<ref name="pmid18488876">{{cite journal | vauthors = Stanworth RD, Jones TH | title = Testosterone for the aging male; current evidence and recommended practice | journal = Clinical Interventions in Aging | volume = 3 | issue = 1 | pages = 25–44 | year = 2008 | pmid = 18488876 | pmc = 2544367 | doi = 10.2147/CIA.S190}}</ref> Nők esetében a magas androgénszint együtt járhat a szabálytalan menstruációs ciklussal.<ref name="pmid17039468">{{cite journal | vauthors = Van Anders SM, Watson NV | title = Menstrual cycle irregularities are associated with testosterone levels in healthy premenopausal women | journal = American Journal of Human Biology | volume = 18 | issue = 6 | pages = 841–44 | year = 2006 | pmid = 17039468 | doi = 10.1002/ajhb.20555 | url = https://deepblue.lib.umich.edu/bitstream/2027.42/83925/1/menstrual_cycle_irregularities_are_associated_with_testosterone_levels_in_healthy_premenopausal_women.pdf | hdl = 2027.42/83925 }}</ref>



====Férfiak====
Férfiaknál a szexuális aktivitás periódusai együttjárnak a magasabb tesztoszteron-szinttel.<ref name="pmid1275688">{{cite journal | vauthors = Kraemer HC, Becker HB, Brodie HK, Doering CH, Moos RH, Hamburg DA | title = Orgasmic frequency and plasma testosterone levels in normal human males | journal = Archives of Sexual Behavior | volume = 5 | issue = 2 | pages = 125–32 | date = Mar 1976 | pmid = 1275688 | doi = 10.1007/BF01541869 }}</ref><ref name=Roney_2003>{{cite journal | vauthors = Roney JR, Mahler SV, Maestripieri D | title = Behavioral and hormonal responses of men to brief interactions with women | journal = Evolution and Human Behavior | year = 2003 | volume = 24 | issue = 6 | pages = 365–75 | doi = 10.1016/S1090-5138(03)00053-9 }}</ref> Szexfilmek nézése után átlagosan 35%-kal nőtt s vér tesztoszteronkoncentrációja (a legmagasabb 60-90 perccel a film vége után volt);<ref>{{cite journal | vauthors = Pirke KM, Kockott G, Dittmar F | title = Psychosexual stimulation and plasma testosterone in man | journal = Archives of Sexual Behavior | volume = 3 | issue = 6 | pages = 577–84 | date = Nov 1974 | pmid = 4429441 | doi = 10.1007/BF01541140 }}</ref> ezenkívül nőtt a motiváció, a versengésre való hajlam és csökkent a kifáradtság.<ref name="pmid4001279">{{cite journal | vauthors = Hellhammer DH, Hubert W, Schürmeyer T | title = Changes in saliva testosterone after psychological stimulation in men | journal = Psychoneuroendocrinology | volume = 10 | issue = 1 | pages = 77–81 | year = 1985 | pmid = 4001279 | doi = 10.1016/0306-4530(85)90041-1 }}</ref> Megfigyelték, hogy a ciklusuk [[Ovuláció|peteérési]] szakaszában lévő nők szagának kitett férfiak hormonszintje magasabb volt, mint a kontrollcsoporté.
Férfiaknál a szexuális aktivitás periódusai együttjárnak a magasabb tesztoszteron-szinttel.<ref name="pmid1275688">{{cite journal | vauthors = Kraemer HC, Becker HB, Brodie HK, Doering CH, Moos RH, Hamburg DA | title = Orgasmic frequency and plasma testosterone levels in normal human males | journal = Archives of Sexual Behavior | volume = 5 | issue = 2 | pages = 125–32 | date = Mar 1976 | pmid = 1275688 | doi = 10.1007/BF01541869 }}</ref><ref name=Roney_2003>{{cite journal | vauthors = Roney JR, Mahler SV, Maestripieri D | title = Behavioral and hormonal responses of men to brief interactions with women | journal = Evolution and Human Behavior | year = 2003 | volume = 24 | issue = 6 | pages = 365–75 | doi = 10.1016/S1090-5138(03)00053-9 }}</ref> Szexfilmek nézése után átlagosan 35%-kal nőtt s vér tesztoszteronkoncentrációja (a legmagasabb 60-90 perccel a film vége után volt);<ref>{{cite journal | vauthors = Pirke KM, Kockott G, Dittmar F | title = Psychosexual stimulation and plasma testosterone in man | journal = Archives of Sexual Behavior | volume = 3 | issue = 6 | pages = 577–84 | date = Nov 1974 | pmid = 4429441 | doi = 10.1007/BF01541140 }}</ref> ezenkívül nőtt a motiváció, a versengésre való hajlam és csökkent a kifáradtság.<ref name="pmid4001279">{{cite journal | vauthors = Hellhammer DH, Hubert W, Schürmeyer T | title = Changes in saliva testosterone after psychological stimulation in men | journal = Psychoneuroendocrinology | volume = 10 | issue = 1 | pages = 77–81 | year = 1985 | pmid = 4001279 | doi = 10.1016/0306-4530(85)90041-1 }}</ref> Megfigyelték, hogy a ciklusuk [[Ovuláció|peteérési]] szakaszában lévő nők szagának kitett férfiak hormonszintje magasabb volt, mint a kontrollcsoporté.
<ref name="pmid20424057">{{cite journal | vauthors = Miller SL, Maner JK | title = Scent of a woman: men's testosterone responses to olfactory ovulation cues | journal = Psychological Science | volume = 21 | issue = 2 | pages = 276–83 | date = Feb 2010 | pmid = 20424057 | doi = 10.1177/0956797609357733 | url = https://semanticscholar.org/paper/71e4403da354af0acb03062f9bb65d543795c1db }}</ref>
<ref name="pmid20424057">{{cite journal | vauthors = Miller SL, Maner JK | title = Scent of a woman: men's testosterone responses to olfactory ovulation cues | journal = Psychological Science | volume = 21 | issue = 2 | pages = 276–83 | date = Feb 2010 | pmid = 20424057 | doi = 10.1177/0956797609357733 | url = https://semanticscholar.org/paper/71e4403da354af0acb03062f9bb65d543795c1db }}</ref>

A lap 2020. január 9., 15:28-kori változata

Testosterone is the primary male sex hormone and an anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair.[1] In addition, testosterone is involved in health and well-being,[2] and the prevention of osteoporosis.[3] Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss.

Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[4] It exerts its action through binding to and activation of the androgen receptor.[4] In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females.[5] As the metabolism of testosterone in males is more pronounced, the daily production is about 20 times greater in men.[6][7] Females are also more sensitive to the hormone.[8]

In addition to its role as a natural hormone, testosterone is used as a medication, for instance in the treatment of low testosterone levels in men, transgender hormone therapy for transgender men, and breast cancer in women.[9] Since testosterone levels decrease as men age, testosterone is sometimes used in older men to counteract this deficiency. It is also used illicitly to enhance physique and performance, for instance in athletes.[10] Sablon:TOC limit


Biológiai hatásai

Általánosságban az androgén hormonok, mint a tesztoszteron elősegítik az androgénreceptorokkal rendelkező szövetekben a fehérjeszintézist, így a szövet növekedését.[11] Úgynevezett virilizáló és anabolikus hatásokat indukál.[12]

  • az anabolikus hatások többek között az izomtömeg és izomerő növekedésével, a csontsűrűség és csontszilárdság fokozódásával járnak valamint fokozzák a csontok hossznövekedését és érését.
  • az androgén hatások a nemi szervek érését okozzák, vagyis a magzatban a pénisz és a herék kialakulását; serdülőkorban pedig az arc- és testszőrzet növekedését, a hang mélyülését, vagyis a másodlagos nemi jellegek kifejlődését.

A tesztoszteron hatásait az életkori megjelenés sorrendjében is felsorolhatjuk. A hatások erőssége a születés után férfiakban és nőkben is nagyban függ a vérben szabadon keringő hormon koncentrációjától és az hatás időtartamának hosszától.

Születés előtt

A tesztoszteron az embrionális fejlődés két szakaszában játszik jelentős szerepet.

Az első periódus a terheség 4-6. hétében játszódik le, amikor a nemi szervek, valamint a húgycső péniszbeli szakasza, a herezacskó kialakulnak. Ebben a szakaszban a dihidritesztoszteron játssza a fő szerepet. Ekkor formálódik a prosztata és az ondóhólyag is.

A második torimeszter során alakulnak ki a magzat nemi jellegei és ebben a folyamatban is kulcsszerepet játszanak az androgén hormonok.[13] Az ekkori hormonszint nagyobb hatással van a későbbi felnőtt nemi viselkedésére, mint a felnőttkori hormonszint.[14] Például a veleszületett mellékvese-megnagyobbodásban szenvedő nőkre inkább jellemző gyerekkorban a fiús játékok kedvelése, felnőttként pedig csökkent heteroszexuális érdeklődést mutatnak a férfiak iránt.[15]

Csecsemőkor

Az androgének hatásai közül a kora csecsemőkoriak a legkevésbé feltártak. A fiúgyermekek születés utáni első heteiben a tesztoszteronszint megnő és néhány hónapig olyan magas, mint amilyen a serdülőkorra jellemző. A 4-7. hónapra a hormonkoncentráció visszaesik az alig detektálható szintre, ami aztán az egész gyermekkorra jellemző marad.[16][17] Ennek az ideiglenes növekedésnek az oka nem ismert; feltételezik, hogy az agy maszkulinizációjához szükséges, ugyanis más szervek változását nem sikerült megfigyelni.[18] Az agy maszkulinizációja úgy történik, hogy a tesztoszteron egyik széngyűrűje aromatizálásával ösztrogénné alakul át, amely át tud hatolni a vér-agy gáton és utána kapcsolódni tud az idegsejtek receptoraihoz; a lányoknál ez a folyamat nem történik meg, mert náluk az alfa-fetoprotein megköti az ösztrogént.[19]

Serdülőkor

A serdülőkor kezdetén a növekvő andrgénszint már érezteti a hatását, mind a fiúkban, mind a lányokban. Ezek közé tartozik a felnőttekre jellemző testszag, a bőr és a haj zsírosabbá válása, a pattanások, a fanszőrzet és a hónaljszőrzet megjelenése, a felgyorsult növekedés.[20]

A tényleges serdülőkori hatások azután jelentkeznek, amikor az androgénszint több hónapja (vagy éve) meghaladja a felnőtt nőkre jellemző értéket. Fiúkban ezek általában késő-serdülőkori hatások, nőkben pedig jelentkezésükhöz hosszabb ideig tartó magas tesztoszteronszint szükséges. A pubertáskori hatások a következők:[20][21]

A herékben a spermatogén szövet kifejlődése, a pénisz (fiúknál) és a csikló (lányoknál) növekedése, erősödő libidó. A növekedési hormon befolyásolása révén az állkapocs, áll, szemöldökcsont megerősödése és az arc kontúrjának változása.[22] A csontfejlődés és a magasságnövekedés befejezése. Utóbbi közvetetten történik az ösztradiol metabolitjain keresztül és fiúkban fokozatosabban zajlik le, mint a lányokban. Az izomtömeg és izomerő növekedése, a vállak szélesedése, a mellkas megnagyobbodása, a hang mélyebbé válása, ádámcsutka kialakulása. A faggyúmirigyek megnagyobbodása (ami pattanások megjelenéséhez vezethet). Az arc bőr alatti zsírrétegének csökkenése. A fanszőrzet kiterjedése a combokra és a köldökig, az arcszőrzet (bajusz, szakáll) növekedése, a fejtetőn a haj gyérülése (ún androgén alopécia), testszőrzet növekedése.

Felnőttkor

A tesztoszteronra szükség van a spermiumok fejlődéshez. Aktiválja a herék Sertoli-sejtjeinek azon génjeit, amelyek elősegítik a spermatogoniumok differenciálódását. Versengési helyzetekben szabályozza a hipotalamusz-agyalapi mirigy-mellékvese rendszer hormonelválasztását.[23] Az androgén hormonok (köztük a tesztoszteron) fokozzák az izomnövekedést. A tesztoszteron befolyásolja a megakariociták és a vérlemezkék tromboxán A2 receptorainak kifejeződését, ezáltal a vérlemezkék aggregációját és a véralvadást.[24][25]

Hatásai a férfiakban egyértelműbben jelentkeznek, bár valószínűleg mindkét nemben fontosak. Az életkor előrehaladtával, ahogy a tesztoszteron szintje visszaesik, úgy a hatások mértéke is csökken.[26]

A magas tesztoszteronkoncentráció nem fokozza a prosztatarák kialakulásának veszélyét. Valószínűleg éppen ellenkezőleg, az alacsony hormonszíntű férfiak kockázata nagyobb és a kialakuló tumor is veszélyesebb.[27][28][29] Idős férfiakban a tesztoszteron közvetetten segít fenntartani a szív- és érrendszer egészségét azzal, hogy gátolja az izptömeg elvesztését, gátolja az elhízást és csökkenti a koleszterinszintet.[30] Nők esetében a magas androgénszint együtt járhat a szabálytalan menstruációs ciklussal.[31]


Férfiaknál a szexuális aktivitás periódusai együttjárnak a magasabb tesztoszteron-szinttel.[32][33] Szexfilmek nézése után átlagosan 35%-kal nőtt s vér tesztoszteronkoncentrációja (a legmagasabb 60-90 perccel a film vége után volt);[34] ezenkívül nőtt a motiváció, a versengésre való hajlam és csökkent a kifáradtság.[35] Megfigyelték, hogy a ciklusuk peteérési szakaszában lévő nők szagának kitett férfiak hormonszintje magasabb volt, mint a kontrollcsoporté. [36]

Females

Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[37] Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling.[38] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.[39]

When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.[40]

Testosterone may prove to be an effective treatment in female sexual arousal disorders,[41] and is available as a dermal patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used as an off-label use to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.[41]

Romantic relationships

Falling in love decreases men's testosterone levels while increasing women's testosterone levels. There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes.[42] However, it is suggested that after the "honeymoon phase" ends—about four years into a relationship—this change in testosterone levels is no longer apparent.[42] Men who produce less testosterone are more likely to be in a relationship[43] or married,[44] and men who produce more testosterone are more likely to divorce;[44] however, causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone levels.[45]

Single men who have not had relationship experience have lower testosterone levels than single men with experience. It is suggested that these single men with prior experience are in a more competitive state than their non-experienced counterparts.[46] Married men who engage in bond-maintenance activities such as spending the day with their spouse and/or child have no different testosterone levels compared to times when they do not engage in such activities. Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities are more relevant to changes in testosterone levels.[47]

Men who produce more testosterone are more likely to engage in extramarital sex.[44] Testosterone levels do not rely on physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are similar.[43] Physical presence may be required for women who are in relationships for the testosterone–partner interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.[48]

Fatherhood

Fatherhood decreases testosterone levels in men, suggesting that the emotions and behavior tied to decreased testosterone promote paternal care. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the parental dyad to raise multiple children simultaneously. This increases the reproductive fitness of the parents, because their offspring are more likely to survive and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced physical and immunological threats.[49] This is particularly beneficial for humans since offspring are dependent on parents for extended periods of time and mothers have relatively short inter-birth intervals.[50]

While extent of paternal care varies between cultures, higher investment in direct child care has been seen to be correlated with lower average testosterone levels as well as temporary fluctuations.[51] For instance, fluctuation in testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated with increased nurturing behavior and better outcomes for the infant.[52]

Motivation

Testosterone levels play a major role in risk-taking during financial decisions.[53][54]

Aggression and criminality

Lásd még: Aggression#Testosterone és Biosocial criminology

Most studies support a link between adult criminality and testosterone. Nearly all studies of juvenile delinquency and testosterone are not significant. Most studies have also found testosterone to be associated with behaviors or personality traits linked with criminality such as antisocial behavior and alcoholism. Many studies have also been done on the relationship between more general aggressive behavior and feelings and testosterone. About half the studies have found a relationship and about half no relationship.[55] Studies have also found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.[56]

Testosterone is significantly discussed in relation to aggression and competitive behavior. There are two theories on the role of testosterone in aggression and competition.[57] The first one is the challenge hypothesis which states that testosterone would increase during puberty, thus facilitating reproductive and competitive behavior which would include aggression.[57] It is therefore the challenge of competition among males of the species that facilitates aggression and violence.[57] Studies conducted have found direct correlation between testosterone and dominance, especially among the most violent criminals in prison who had the highest testosterone levels.[57] The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.[57]

The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[58][59] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.[58] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[60] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.[61][62][63][64][65]

The rise in testosterone levels during competition predicted aggression in males but not in females.[66] Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression.[67] Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations.[68] Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and physical violence.[69] Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli.[70] Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.[71]

Testosterone might encourage fair behavior. For one study, subjects took part in a behavioral experiment where the distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a rejection of their offer to a minimum. Two later studies have empirically confirmed these results.[72][73][74] However men with high testosterone were significantly 27% less generous in an ultimatum game.[75] The Annual NY Academy of Sciences has also found anabolic steroid use (which increases testosterone) to be higher in teenagers, and this was associated with increased violence.[76] Studies have also found administered testosterone to increase verbal aggression and anger in some participants.[77]

A few studies indicate that the testosterone derivative estradiol (one form of estrogen) might play an important role in male aggression.[55][78][79][80] Estradiol is known to correlate with aggression in male mice.[81] Moreover, the conversion of testosterone to estradiol regulates male aggression in sparrows during breeding season.[82] Rats who were given anabolic steroids that increase testosterone were also more physically aggressive to provocation as a result of "threat sensitivity".[83]

Brain

The brain is also affected by this sexual differentiation;[13] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[84]

There are some differences between a male and female brain (possibly the result of different testosterone levels), one of them being size: the male human brain is, on average, larger.[85] Men were found to have a total myelinated fiber length of 176 000 km at the age of 20, whereas in women the total length was 149 000 km (approx. 15% less).[86]

No immediate short term effects on mood or behavior were found from the administration of supraphysiologic doses of testosterone for 10 weeks on 43 healthy men.[87] A correlation between testosterone and risk tolerance in career choice exists among women.[53][88]

Attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer's type,[89][90][91][92] a key argument in life extension medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone,[93] where both hypo- and hypersecretion (deficient- and excessive-secretion) of circulating androgens have negative effects on cognition.

Immune system and inflammation

Testosteone deficiency is associated with an increased risk of metabolic syndrome, cardiovascular disease and mortality, which are also sequelae of chronic inflammation.[94] Testosterone plasma concentration inversely correlates to multiple biomarkers of inflammation including CRP, interleukin 1 beta, interleukin 6, TNF alpha and endotoxin concentration, as well as leukocyte count.[94] As demonstrated by a meta-analysis, substitution therapy with testosterone results in a significant reduction of inflammatory markers.[94] These effects are mediated by different mechanisms with synergistic action.[94] In androgen-deficient men with concomitant autoimmune thyroiditis, substitution therapy with testosterone leads to a decrease in thyroid autoantibody titres and an increase in thyroid's secretory capacity (SPINA-GT).[95]

Medical use

Bővebben: Testosterone (medication)

Testosterone is used as a medication for the treatment of males with too little or no natural testosterone production, certain forms of breast cancer,[9] and gender dysphoria in transgender men. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. Decline of testosterone production with age has led to interest in androgen replacement therapy.[96] It is unclear if the use of testosterone for low levels due to aging is beneficial or harmful.[97]

Testosterone is included in the World Health Organization's list of essential medicines, which are the most important medications needed in a basic health system.[98] It is available as a generic medication.[9] The price depends on the form of testosterone used.[99] It can be administered as a cream or transdermal patch that is applied to the skin, by injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.[9]

Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[9] Serious side effects may include liver toxicity, heart disease, and behavioral changes.[9] Women and children who are exposed may develop virilization.[9] It is recommended that individuals with prostate cancer not use the medication.[9] It can cause harm if used during pregnancy or breastfeeding.[9]

Biological activity

Steroid hormone activity

The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[100][101] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[102][103][104]

Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[105] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.

Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond similarly to similar levels. Greatly differing amounts of testosterone prenatally, at puberty, and throughout life account for a share of biological differences between males and females.

The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion).[106] In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.[107]

Neurosteroid activity

Testosterone, via its active metabolite 3α-androstanediol, is a potent positive allosteric modulator of the GABAA receptor.[108]

Testosterone has been found to act as an antagonist of the TrkA and p75NTR, receptors for the neurotrophin nerve growth factor (NGF), with high affinity (around 5 nM).[109][110][111] In contrast to testosterone, DHEA and DHEA sulfate have been found to act as high-affinity agonists of these receptors.[109][110][111]

Testosterone is an antagonist of the sigma σ1 receptor (Ki = 1,014 or 201 nM).[112] However, the concentrations of testosterone required for binding the receptor are far above even total circulating concentrations of testosterone in adult males (which range between 10 and 35 nM).[113]

Biochemistry

Human steroidogenesis, showing testosterone near bottom.[114]

Biosynthesis

Like other steroid hormones, testosterone is derived from cholesterol (see figure).[115] The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids.[116] In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.

The largest amounts of testosterone (>95%) are produced by the testes in men,[1] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[117] In the testes, testosterone is produced by the Leydig cells.[118] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).

Regulation

Hypothalamic–pituitary–testicular axis

In males, testosterone is synthesized primarily in Leydig cells. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase.[119]

The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (see figure to the right).[120] When testosterone levels are low, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH. These latter two hormones stimulate the testis to synthesize testosterone. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively.

Factors affecting testosterone levels may include:

  • Age: Testosterone levels gradually reduce as men age.[121][122] This effect is sometimes referred to as andropause or late-onset hypogonadism.[123]
  • Exercise: Resistance training increases testosterone levels,[124] however, in older men, that increase can be avoided by protein ingestion.[125] Endurance training in men may lead to lower testosterone levels.[126]
  • Nutrients: Vitamin A deficiency may lead to sub-optimal plasma testosterone levels.[127] The secosteroid vitamin D in levels of 400–1000 IU/d (10–25 µg/d) raises testosterone levels.[128] Zinc deficiency lowers testosterone levels[129] but over-supplementation has no effect on serum testosterone.[130]
  • Weight loss: Reduction in weight may result in an increase in testosterone levels. Fat cells synthesize the enzyme aromatase, which converts testosterone, the male sex hormone, into estradiol, the female sex hormone.[131] However no clear association between body mass index and testosterone levels has been found.[132]
  • Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[133] Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[134] Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[135][136][137] Licorice can decrease the production of testosterone and this effect is greater in females.[138]

Distribution

The plasma protein binding of testosterone is 98.0 to 98.5%, with 1.5 to 2.0% free or unbound.[139] It is bound 65% to sex hormone-binding globulin (SHBG) and 33% bound weakly to albumin.[140]

Plasma protein binding of testosterone and dihydrotestosterone
Compound Group Level (nM) Free (%) SHBG (%) CBG (%) Albumin (%)
Testosterone Adult men 23.0 2.23 44.3 3.56 49.9
Adult women
  Follicular phase 1.3 1.36 66.0 2.26 30.4
  Luteal phase 1.3 1.37 65.7 2.20 30.7
  Pregnancy 4.7 0.23 95.4 0.82 3.6
Dihydrotestosterone Adult men 1.70 0.88 49.7 0.22 39.2
Adult women
  Follicular phase 0.65 0.47 78.4 0.12 21.0
  Luteal phase 0.65 0.48 78.1 0.12 21.3
  Pregnancy 0.93 0.07 97.8 0.04 21.2
Sources: [139][141]

Metabolism

Sablon:Testosterone metabolism mini

Both testosterone and 5α-DHT are metabolized mainly in the liver.[142][143] Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively.[142] An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order.[142][143][144] Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone.[142][143] The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile.[142][143][144] Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[143]

In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[142][143] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[142][143] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[142][143] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[145][146] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[144]

In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6.[147] 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations.[147] The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism.[147] In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites.[147][148] Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.[147]

Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues.[143] Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase.[1][143][149][150] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[151] skin, hair follicles, and brain[152] and aromatase is highly expressed in adipose tissue, bone, and the brain.[153][154] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[144] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[155] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[156]

Levels

Total levels of testosterone in the body are 264 to 916 ng/dL in men age 19 to 39 years,[157] while mean testosterone levels in adult men have been reported as 630 ng/dL.[158] Levels of testosterone in men decline with age.[157] In women, mean levels of total testosterone have been reported to be 32.6 ng/dL.[159][160] In women with hyperandrogenism, mean levels of total testosterone have been reported to be 62.1 ng/dL.[159][160]

Sablon:Testosterone levels in males and females

Total testosterone levels in males throughout life
Life stage Tanner stage Age range Mean age Levels range Mean levels
Child Stage I <10 years – <30 ng/dL 5.8 ng/dL
Puberty Stage II 10–14 years 12 years <167 ng/dL 40 ng/dL
Stage III 12–16 years 13–14 years 21–719 ng/dL 190 ng/dL
Stage IV 13–17 years 14–15 years 25–912 ng/dL 370 ng/dL
Stage V 13–17 years 15 years 110–975 ng/dL 550 ng/dL
Adult – ≥18 years – 250–1,100 ng/dL 630 ng/dL
Sources: [161][161][162][158][163][164]
Reference ranges for blood tests, showing adult male testosterone levels in light blue at center-left.


Measurement

Testosterone's bioavailable concentration is commonly determined using the Vermeulen calculation or more precisely using the modified Vermeulen method,[165][166] which considers the dimeric form of sex-hormone-binding-globulin.[167]

Both methods use chemical equilibrium to derive the concentration of bioavailable testosterone: in circulation testosterone has two major binding partners, albumin (weakly bound) and sex-hormone-binding-globulin (strongly bound). These methods are described in detail in the accompanying figure.

  • Dimeric sex-hormone-binding-globulin with its testosterone ligands
    Dimeric sex-hormone-binding-globulin with its testosterone ligands
  • Two methods for determining concentration of bioavailable testosterone.
    Two methods for determining concentration of bioavailable testosterone.

History

A testicular action was linked to circulating blood fractions – now understood to be a family of androgenic hormones – in the early work on castration and testicular transplantation in fowl by Arnold Adolph Berthold (1803–1861).[168] Research on the action of testosterone received a brief boost in 1889, when the Harvard professor Charles-Édouard Brown-Séquard (1817–1894), then in Paris, self-injected subcutaneously a "rejuvenating elixir" consisting of an extract of dog and guinea pig testicle. He reported in The Lancet that his vigor and feeling of well-being were markedly restored but the effects were transient,[169] and Brown-Séquard's hopes for the compound were dashed. Suffering the ridicule of his colleagues, he abandoned his work on the mechanisms and effects of androgens in human beings.

In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them.[170] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.

Nobel Prize winner, Leopold Ruzicka of Ciba, a pharmaceutical industry giant that synthesized testosterone.

The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)".[171] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.[172][173]

The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[174] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[175] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[173][176] Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.

The partial synthesis in the 1930s of abundant, potent testosterone esters permitted the characterization of the hormone's effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Allan Kenyon's group[177] was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The Golden Age of Steroid Chemistry",[178] and work during this period progressed quickly. Research in this golden age proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.[179]

Other animals

Testosterone is observed in most vertebrates. Testosterone and the classical nuclear androgen receptor first appeared in gnathostomes (jawed vertebrates).[180] Agnathans (jawless vertebrates) such as lampreys do not produce testosterone but instead use androstenedione as a male sex hormone.[181] Fish make a slightly different form called 11-ketotestosterone.[182] Its counterpart in insects is ecdysone.[183] The presence of these ubiquitous steroids in a wide range of animals suggest that sex hormones have an ancient evolutionary history.[184]

See also

References

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  172. ↑ (1935) „Umwandlung des Dehydroandrosterons in Androstendiol und Testosterone; ein Weg zur Darstellung des Testosterons aus Cholestrin” (german nyelven). Hoppe-Seyler's Z Physiol Chem 237 (2), 89–97. o. DOI:10.1515/bchm2.1935.237.1-3.89.  
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  174. ↑ (1935) „Uber die Umwandlung des Dehydroandrosterons in Androstenol-(17)-one-(3) (Testosterone); um Weg zur Darstellung des Testosterons auf Cholesterin (Vorlauf Mitteilung). [The conversion of dehydroandrosterone into androstenol-(17)-one-3 (testosterone); a method for the production of testosterone from cholesterol (preliminary communication)]” (german nyelven). Chemische Berichte 68 (9), 1859–62. o. DOI:10.1002/cber.19350680937.  
  175. ↑ (1935) „Uber die kristallinische Herstellung des Testikelhormons, Testosteron (Androsten-3-ol-17-ol) [The crystalline production of the testicle hormone, testosterone (Androsten-3-ol-17-ol)]” (german nyelven). Helvetica Chimica Acta 18, 1264–75. o. DOI:10.1002/hlca.193501801176.  
  176. ↑ (1995. február 1.) „The history of synthetic testosterone”. Scientific American 272 (2), 76–81. o. DOI:10.1038/scientificamerican0295-76. PMID 7817189.  
  177. ↑ (1940. február 1.) „A comparative study of the metabolic effects of testosterone propionate in normal men and women and in eunuchoidism”. Endocrinology 26 (1), 26–45. o. DOI:10.1210/Endo-26-1-26.  
  178. ↑ (1999. július 1.) „The steroid story of Jenapharm: from the late 1940s to the early 1970s”. Steroids 64 (7), 439–45. o. DOI:10.1016/S0039-128X(99)00003-3. PMID 10443899.  
  179. ↑ The Male Hormone. New York: Harcourt, Brace (1945) 
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  182. ↑ An introduction to behavioral endocrinology. Sunderland, Mass: Sinauer Associates, 143. o. (2005). ISBN 978-0-87893-617-5 
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Further reading

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